The goal is this proposal is to investigate the effect of organophosphorus-induced delayed neurotoxicity (OPIDN) on peripheral nerve and spinal cord electrophysiology. OPIDN is characterized by a slient period 6-14 days before onset of clinical signs and nerve degeneration in both man and sensitive animals. Pathological changes include degeneration in both the peripheral and central nervous system with the distal parts of the longest nerve fibers, both motor and sensory, affected first. In this proposal, the cat will be used as a test animal for recording electrophysiological changes induced by a single dermal dose of tri-o-cresyl phosphate (TOCP), an organophosphorus ester known to induce delayed neurotoxicity. Peripheral nerve function will be assessed using muscle contractile responses to nerve evoked stimuli and stimulus bound repetition which is a nerve terminal related phenomenon. Spinal cord function is to be quantified in terms of both absolute values of monosynaptic reflex responses, and input-output characteristics of the reflex to determine relative amount of transmitter turnover in the spinal cord. Electrophysiological data from animals with OPIDN has been limited. In this investigation, I hope to more clearly elucidate the delayed neurotoxic effects of organophosphorus esters on spinal cord and peripheral nerve physiology in a mammalian species.